Figure 4
(A) Dysferlin associates with plasma and vesicle membranes. Other proteins including TRIM72, AHNAK, and S100A10:ANX2 are mostly cytosolic. (B) Membrane rupture causes a local Ca2+ influx, binding to and activating Ca2+-sensitive proteins such as dysferlin and ANX2. This enables multiple interactions between the proteins and causes recruitment of TRIM72 and AHNAK by dysferlin and S100A10:ANX2 to vesicle surfaces. (C) Ca2+-dependent protein–protein interactions recruit vesicles such as enlargosomes to the injured plasma membrane facilitated by the complete dysferlin complex that spans the vesicle-plasma membrane space. (D) Multiple vesicles containing dysferlin and interacting proteins accumulate at the injured site forming a patch across the membrane lesion.
Model of dysferlin-mediated vesicle fusion membrane repair

(A) Dysferlin associates with plasma and vesicle membranes. Other proteins including TRIM72, AHNAK, and S100A10:ANX2 are mostly cytosolic. (B) Membrane rupture causes a local Ca2+ influx, binding to and activating Ca2+-sensitive proteins such as dysferlin and ANX2. This enables multiple interactions between the proteins and causes recruitment of TRIM72 and AHNAK by dysferlin and S100A10:ANX2 to vesicle surfaces. (C) Ca2+-dependent protein–protein interactions recruit vesicles such as enlargosomes to the injured plasma membrane facilitated by the complete dysferlin complex that spans the vesicle-plasma membrane space. (D) Multiple vesicles containing dysferlin and interacting proteins accumulate at the injured site forming a patch across the membrane lesion.

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